Apocrine cells reflect a metaplastic alteration of native epithelial cells and are a usual component of fibrocystic change. The apocrine phenotype is observed in a wide spectrum of breast epithelial lesions spanning benign metaplasias to carcinoma (1-3). The reported incidence of apocrine carcinoma varies considerably, ranging from less than 1% to 60%, reflecting varying diagnostic criteria which includes purely light microscopic features as well as reliance on antigenic markers (1). The latter specifically refers to immunohistochemical detection of GCDFP, as this protein is produced by metaplastic apocrine cells (4).

Apocrine carcinomas occur over a wide age range, although predominantly in the 6th and 7th decades. Grossly, these tumors are generally indistinguishable from invasive breast carcinomas, NOS and they present in a similar manner (1). Microscopically, apocrine carcinomas are composed of cords, sheets, and occasionally tubules of neoplastic cells (1,3). Cytologically, the tumor cells are large with relatively abundant, granular, eosinophilic cytoplasm and distinct cell margins; vesicular nuclei with prominent eosinophilic cytoplasm are characteristic (1,3). If an in-situ component is present, it is also usually of the apocrine type, as in the present case. Immunohisto-chemically, the majority of apocrine carcinomas express GCDFP-15 and androgen receptor, and lack immunohistochemically detectable ER and PR (1,3,5). The ultrastructural features of these carcinomas are variable but typically include the presence of mitochondria which are often numerous. Membrane-bound intracytoplasmic osmiophilic bodies are also described, and reportedly correspond to either the cytoplasmic eosinophilic granularity seen microscopically (6), or to the cellular GCDFP-15 content (7).

The prognosis of apocrine carcinoma is not clearly any different from invasive mammary carcinomas, NOS (3), although some reports suggest a somewhat better prognosis for this variant (1).